Neoplasia Oncogene vs Tumor Suppressor

Oncogenes and Tumor Suppressor Genes

Acquired Immunity - Part 2: Lymphocyte Ontogeny, Activation, and Tolerance

Lecture 21 - Oncogenes and Tumor Suppressor Genes

Lecture 20 - Regulation of Gene Expression and Oncogenes

PSYCH 317: Ontogeny of Social Behaviour

Cancer Biology I - Chapter 6: Oncogenes

Ontogeny of EEG from Childhood to Adult

H2: Oncogenen en tumor suppressor genen

[04.01a] Oncogenic Viruses (Part 1) V2.pdf

[04.01b] Oncogenic Viruses (Part 2) V2.1.pdf

Lecture 12: Oncogenes 1- start here tmr

Lecture 13: Oncogenes 2

Oncogenes, Tumor Suppressors, Carcinogens & Tumor Markers

Onkogener

Genetics of Oncogenes (LEC)

Lecture 2 - Oncogenes

Question 3: Logical Deduction of Epigenetic Tool Use Scenario: A hematologic malignancy is driven by the over-expression of the c-MYC oncogene. You are comparing two therapeutic strategies: using a BET inhibitor (an epigenetic reader tool) versus an EZH2 inhibitor (an epigenetic writer tool). Task: Based on their molecular mechanisms, deduce which tool would be more effective for immediate suppression of the MYC protein and explain why. Conversely, describe what would happen to the chromatin landscape if you used the writer inhibitor (EZH2i) on a system with H3K27me3-mediated repression.

Question 5: Methodology for Distinguishing lncRNA Functional Modes In the study of lung cancer vulnerabilities, Esposito et al. (2022) noted that genomic deletion (CRISPR-del) of a lncRNA locus cannot distinguish between a DNA-dependent (e.g., an enhancer element) or an RNA-dependent (the transcript itself) mechanism. Task: Apply the methodology found in the paper to a hypothetical scenario: If you have a screen hit at the candidate 205 (LINC00115) locus, describe how you would use Antisense Oligonucleotides (ASOs) to prove that the oncogenic phenotype is mediated by the RNA transcript rather than the underlying DNA sequence.

MB2 - oncogenes